Alcohol abuse by adolescents and teenagers is a continuing problem in the United States. The effects of chronic alcohol consumption on prepubertal development in the human male are unknown. Studies conducted in rats and mice report that chronic ethanol exposure delays the onset of puberty. The mechanism(s) by which ethanol consumption interacts with the hypothalamic-pituitary-testicular axis during pubertal development is not well defined. It is proposed that alcohol delays the onset of puberty by disrupting hypothalamic gonadotropin releasing hormone (GnRH) secretion and/or anterior pituitary secretion of luteinizing hormone (LH). Our hypothesis postulates that prepubertal rats chronically consuming ethanol have decreased pulsatile secretion of LH due to depressed hypothalamic GnRH secretion. The Specific Aims of this study are to determine whether chronic ethanol consumption alters 1) pulsatile LH secretion from the anterior pituitary gland or 2) hypothalamic GnRH secretion, and whether these changes are correlated with delayed puberty in the male rat. Prepubertal rats will consume ethanol (6% v/v; treated) or an isocaloric dextrin-maltose control diet for 30 days. Separate studies will be conducted to evaluate both anterior pituitary and hypothalamic function. Serial blood samples will be collected in all studies and LH concentrations measured by radioimmunoassay. Pulsatile LH secretion from the anterior pituitary gland will be evaluated on days 7, 14, 21, and 30 following initiation of ethanol consumption. To ensure that the anterior pituitary gland is responsive to GnRH, rats will be treated with exogenous GnRH 7, 14, 21, and 30 days following initiation of treatments. The time, magnitude and duration of GnRH-stimulated LH secretion will be utilized to characterize responsiveness of the anterior pituitary gland. Regulation of hypothalamic GnRH secretion will be evaluated by two procedures. In the first experiment, the excitatory amino acid N-methyl-D-aspartate (NMDA) will be used to stimulate GnRH secretion from the hypothalamus. Concentrations of LH in the serial blood samples will be utilized to evaluate GnRH secretion, since LH is released in direct proportion to the magnitude of the GnRH stimulus. In the second experiment, the ability of opioid peptides to decrease GnRH secretion will be examined. Rats will receive naloxone (an opioid antagonist) implants, and the ability of the hypothalamus to secrete GnRH in response to NMDA will be examined in control and treated rats. Results obtained from these studies will provide a greater understanding of the interaction between chronic alcohol consumption and the hypothalamic-pituitary axis of the prepubertal male. These studies will provide information that will be useful in determining the potential health risks to adolescents chronically consuming ethanol. In addition, data obtained from these studies will provide the basis for future studies directed at elucidation of the specific mechanism(s) by which chronic ethanol consumption depresses hypothalamic-pituitary-testicular function and leads to a delayed onset of puberty.